1. Immunity Introduction to specific immunity

2. Introduction to Immunity Immunity is a physiological reaction of the body to factors it considers threatening and foreign to it Immune system can distinguish ‘self’ from ‘non-self’ A factor which evokes the immune response is referred to as an Antigen (or immunogen) Antigens may be isolated molecules or may be molecules at the surface of an invading cell Antigens are usually exogenous, but may be endogenous (i.e. part of the auto immune reaction)

3. Non Specific or Specific Immunity? Non-specific = Innate = Inherited defence mechanisms Specific = Acquired = Prior exposure Non-specific Immunity Eyes, Mouth, Nose Lungs, Skin, Stomach Reproductive System Large intestine, Urinary Tract

4. Non-Specific Immunity Eyes e.g. Lysozyme in tear fluid, flushing action Mouth e.g. Lysozyme in saliva, flushing action Nose e.g. sneezing, nose hairs

5. Non-Specific Immunity Lungs e.g. coughing, muco-ciliary clearance Skin e.g. waterproof skin/physical barrier, sebum and acid pH

6. Non-Specific Immunity Stomach e.g. HCl in gastric juice Reproductive System e.g. competition from harmless bacteria in vagina, acid pH of vagina, antibacterial proteins in semen

7. Non-Specific Immunity Large intestine e.g. competition from normal gut flora Urinary Tract e.g. directional flow and flushing action of urine

8. Non Specific Responses: Phagocytosis and Inflammation Phagocytosis Phagocytes contain lysosomes with enzymes Phagocytes adhere to, engulf and destroy (digest and recycle) micro-organisms

9. Phagocytosis Phagocytic cells include Neutrophils Macrophages Monocytes

11. Phagocytosis Neutrophils Generated in bone marrow Comprise 50-70% of total white cell count Recognise and phagocytose unwanted or foreign materials, then die

12. Phagocytosis Macrophages Highly mobile cells that migrate through connective tissue Widely distributed throughout body tissues Role is to phagocytose large bacteria and dead body cells

13. Phagocytosis Monocytes Multiple roles in immune function: Replenish resident macrophages In response to inflammation signals, can move quickly to sites of infection in the tissues and differentiate into macrophages Have large kidney shaped nucleus [Recognition by phagocytes can be enhanced by the binding of antibodies to the bacteria]

14. Phagocytosis Phagocytes are attracted to the micro-organism by a process known as Chemotaxis Neutrophils and monocytes are able to squeeze through tiny gaps between adjacent endothelial cells (Diapedesis)

15. Phagocytosis What intracellular structures (necessary for digesting ingested particles) are highlighted in the diagram ? What happens to the bacterium?

16. Inflammation Mast cells release histamine Histamine: Increases blood flow via vasodilatation Increases capillary permeability  Both processes result in more phagocytes to the area

17. Inflammation and Phagocytosis Identify (on the diagram below): The site of bacterial entry? What has coated the bacterium? Where have the antibodies come from? Where is the phagocytic cell coming from? What has activated the mast cells? What chemical has the mast cell released? What effects has this chemical had on the capillary? What is diapedesis?

18. Diagram: Immune Response

19. Characteristics of Inflammation Redness Warmth Swelling Pain (+ or – Pus)

20. Leucocytes Leucocytes are attracted to an area of inflammation by Chemotaxis In which order do the leucocytes arrive at the area of inflammation?

21. Additional points What are endotoxins? What are Cytokines (and some examples)? What is the Complement system? What are Interferons?

22. Specific or Acquired Immunity The immune system also produces very specific responses Antigens / Immunogens induce specific immune responses. Antigens include: foreign proteins, bacteria, viruses, foreign cells

23. Lymphocytes Specific immunity involves Lymphocytes Lymphocytes are derived from stem cells in the bone marrow Lymphocytes replace themselves by cell division

24. T Lymphocytes Lymphocytes that seed the thymus become T lymphocytes (the thymus atrophies after puberty) T lymphocytes do not secrete antibodies

25. Types of T Lymphocytes Helper T cells * Activation of other defence cells (e.g. production of antibodies by B cells) * Regulate the response of both T Killer cells and B cells Suppressor T Cells * Inhibit T and B cell activities * Affect the amount of antibodies secreted and moderate immune response (‘switch off’ immunity)

26. Types of Lymphocytes Killer T cells * Destroy specific cells with antigens on their surface * Must be in actual contact with their victim cells * Defend against viral and fungal infections T Lymphocytes provide cell mediated immunity

27. B Lymphocytes B lymphocytes are processed in the bone marrow B lymphocytes combat bacterial infections as well as viral infections by secreting antibodies into the blood and lymph. Antibodies bind to Antigens B lymphocytes provide humoral immunity (blood and lymph are body fluids or humors)

28. B Lymphocytes

29. B lymphocytes when stimulated produce: a) Memory cells b) Plasma cells Antibodies Antibody proteins are also known as immuno-globulins (or gamma-globulins) [Immuno globulins may be found in, for example, colostrum]

30. Antibodies lgGMain form of antibodies in circulation: production increased after immunization; secreted during secondary response lgAMain antibody type in external secretions, such as saliva & mother’s milk lgEResponsible for allergic symptoms in immediate hypersensitivity reactions lgMFunction as antigen receptors on lymphocyte surface prior to immunization; secreted during primary response lgDFunction as antigen receptors on lymphocyte surface prior to immunization; other functions unknown

31. B and T lymphocytes

32. Primary and Secondary Immune Response On first exposure to a pathogen, the immune response is insufficient to combat the disease There is a latent period in which there are insufficient amounts of specific antibodies On second exposure to the same antigen antibody production is much more rapid

33. Immune Response

34. Application to practice You might like to think about relevant cases from practice (maintaining confidentiality, of course). You could also consider own history with regard to infections / vaccinations / problems with immunity (for example, when have you found yourself prone to infections?). For those with an interest in mental health, what is Agranulocytosis and what anti-psychotic drug has this listed as an adverse effect? What are the arguments for allowing children to be exposed to ‘childhood infections’?